ReviewThorax1998
Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists.
Review in Thorax, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 83 citations in OpenAlex.
- Selective Blockade of TNFR1 Improves Clinical Disease and Bronchoconstriction in Experimental RSV Infection.Viruses · 2020Article
- Estrogen receptors differentially regulate intracellular calcium handling in human nonasthmatic and asthmatic airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Mechanisms underlying TNFα-induced enhancement of force generation in airway smooth muscle.Physiological reports · 2019Article
- A TNFRSF14-FcɛRI-mast cell pathway contributes to development of multiple features of asthma pathology in mice.Nature communications · 2016Article
- cAMP-mediated secretion of brain-derived neurotrophic factor in developing airway smooth muscle.Biochimica et biophysica acta · 2015Article
- Airway smooth muscle in asthma: just a target for bronchodilation?Clinics in chest medicine · 2012Review
- PPARγ Ligands Regulate Noncontractile and Contractile Functions of Airway Smooth Muscle: Implications for Asthma Therapy.PPAR research · 2012Article
- Molecular expression and functional role of canonical transient receptor potential channels in airway smooth muscle cells.Advances in experimental medicine and biology · 2011Review
- Effect of proinflammatory cytokines on regulation of sarcoplasmic reticulum Ca2+ reuptake in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2009Article
- HSP20 phosphorylation and airway smooth muscle relaxation.Cell health and cytoskeleton · 2009Article
- Allergic airway responses in obese mice.American journal of respiratory and critical care medicine · 2007Article
- Activation of tumor necrosis factor receptor 1 in airway smooth muscle: a potential pathway that modulates bronchial hyper-responsiveness in asthma?Respiratory research · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The important pathophysiological features of the airways in asthma include exaggerated narrowing to bronchoconstrictor agonists and attenuated relaxation to beta adrenoceptor stimulation. These physiological perturbations are associated with inflammation and remodelling of the airways, the latter including an increase in airway smooth muscle cell mass, disruption of the airway epithelium, and changes in the airway tissue extracellular matrix. Recent evidence suggests that cytokines, important molecules modulating airway inflammation, also directly decrease airway smooth muscle responsiveness to beta adrenergic agents, stimulate cytokine secretion, inhibit or promote airway smooth muscle proliferation, and "prime" airway smooth muscle to become hyperresponsive to bronchoconstrictors. Characterisation of the cellular and biochemical events that are involved in activation of airway smooth muscle is likely to be the major consideration in the design of future therapies for asthma. Because calcium is an essential regulatory element for cell growth and cell contraction, it is likely that alterations in calcium mobilisation may, in part, play a role in creating an airway smooth muscle phenotype that is hyperresponsive to contractile agonists. Further studies will be required to determine the precise mechanisms involved in cytokine modulation of calcium homeostasis in airway smooth muscle.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.